Εξειδίκευση τύπου :	Άρθρο σε επιστημονικό περιοδικό
Τίτλος:	Ptch1 overexpression drives skin carcinogenesis and developmental defects in K14Ptch FVB mice
Δημιουργός/Συγγραφέας:	Kang H.C. Wakabayashi Y. Jen K.-Y. Mao J.-H. [EL] Ζουμπουρλής, Βασίλης[EN] Zoumpourlis, Vassilis Del Rosario R. Balmain A.
Εκδότης:	Nature Publishing Group
Ημερομηνία:	2013
Γλώσσα:	Αγγλικά
ISSN:	0022-202X
DOI:	10.1038/jid.2012.419
Περίληψη:	Ptch1 is a key regulator of embryonic development, acting through the sonic hedgehog (SHH) signaling pathway. Ptch1 is best known as a tumor suppressor, as germline or somatic mutations in Ptch1 lead to the formation of skin basal cell carcinomas. Here we show that Ptch1 also acts as a lineage-dependent oncogene, as overexpression of Ptch1 in adult skin in K14Ptch FVB transgenic mice synergizes with chemically induced Hras mutations to promote squamous carcinoma development. These effects were not because of aberrant activation of SHH signaling by the K14Ptch FVB transgene, as developmental defects in the highest expressing transgenic lines were consistent with the inhibition of this pathway. Carcinomas from K14Ptch FVB transgenic mice had only a small number of nonproliferative Ptch1 transgene-positive cells, suggesting that the Ptch1 transgene is not required for tumor maintenance, but may have a critical role in cell-fate determination at the initiation stage.
Τίτλος πηγής δημοσίευσης:	Journal of Investigative Dermatology
Τόμος/Κεφάλαιο:	133
Τεύχος:	5
Σελίδες:	1311-1320
Θεματική Κατηγορία:	[EL] Βιολογία (Γενικά)[EN] Biology (General) [EL] Νεοπλάσματα. Όγκοι. Ογκολογία (περ. Καρκίνος, κακινογόνες ουσίες)[EN] Neoplasms. Tumors. Oncology (Incl.cancer, carcinogens)
Αξιολόγηση από ομότιμους (peer reviewed):	Ναι
Κάτοχος πνευματικών δικαιωμάτων:	© 2013 The Society for Investigative Dermatology.
Όροι και προϋποθέσεις δικαιωμάτων:	All Open Access, Bronze, Green
Σημειώσεις:	National Institutes of Health, NIH; National Cancer Institute, NCI: 2U01 CA08422-06, 5P01AR050440; National Institute of Arthritis and Musculoskeletal and Skin Diseases, NIAMS; Japan Society for the Promotion of Science, JSPS: 23241066, 23590454. These studies were supported by National Cancer Institute Mouse Models of Human Cancer Consortium grant 2U01 CA08422-06 to AB and Program Project Grant (PPG) 5P01AR050440 from the US National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health. AB acknowledges support from the Barbara Bass Bakar Chair of Cancer Genetics.
Εμφανίζεται στις συλλογές:	Ινστιτούτο Χημικής Βιολογίας - Επιστημονικό έργο